NATURE IMMUNOLOGY自然·免疫学
NATURE IMMUNOLOGY(英文缩写 NAT IMMUNOL),ISSN 1529-2908,eISSN 1529-2916,中文译名:自然·免疫学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 31.250 | Q1 |
| 2022 | 30.500 | Q1 |
| 2023 | 27.700 | Q1 |
| 2024 | 27.600 | Q1 |
| 2025 | 26.500 | Q1 |
NATURE IMMUNOLOGY 最新收录文献
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1. Remodeling of a distal IRF4 element spurs human regulatory T cell instability under inflammatory conditions.
PMID:日期:2026-09-24该文献暂无摘要。
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6. Metastasis enables immunogenicity through migrasome-mediated antigen release.
PMID:日期:2026-09-22Antigen release is a critical step in initiating antitumor immune responses, yet its regulation during metastasis is not well understood. Here we show that circulating tumor cells undergoing vascular migration produce migrasomes that serve as a metastasis-specific mechanism of antigen release. These migrasomes are enriched in tumor-associated antigens, including cancer-testis and mutated antigens, and are captured efficiently by antigen-presenting cells in secondary lymphoid organs, where they undergo cross-presentation to elicit CD8 T cell-mediated immune responses that constrain metastatic progression. Genetic inhibition of migrasome formation enhances metastasis, while administration of purified cancer-derived migrasomes restores immune-mediated suppression of metastatic growth. These findings show paradoxically that metastasis can enhance tumor immunogenicity through migrasome-mediated antigen release, highlighting a link between cancer dissemination and immune activation and establishing migrasomes as a distinct and potent platform for endogenous tumor antigen delivery.
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7. Deletion of a distal IRF4 element prevents inflammation-induced reprogramming of human regulatory T cell fate.
PMID:日期:2026-09-21Regulatory T (T) cells in mice can lose lineage identity and acquire proinflammatory functions, but whether human T cells are similarly susceptible to cytokine-driven destabilization remains unclear. Here we established an in vitro model of human T cell destabilization defined by silencing of the lineage-specifying transcription factor FOXP3, loss of suppressive function and acquisition of proinflammatory activity. Single-cell chromatin accessibility and transcriptomic profiling revealed a genome-wide increase in accessibility at AP-1-binding sites, including a putative regulatory element distal to IRF4. Increased accessibility at this element correlated with increased IRF4 expression during T cell destabilization, and its excision conferred resistance to inflammatory cytokine-induced reprogramming. Conversely, forced expression of IRF4 together with BATF promoted T cell destabilization. These data identify a distal IRF4 regulatory element as a critical node enabling heightened AP-1-IRF4 cooperative activity to drive T cell destabilization, with implications for the design of more stable and effective T cell-based therapies.
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8. Spatiotemporal single-cell profiling reveals T cell clonal dynamics and phenotypic plasticity in human graft-versus-host disease.
PMID:日期:2026-09-17Allogeneic hematopoietic cell transplantation cures hematologic diseases but is limited by acute graft‑versus‑host disease. How human T cell clones drive epithelial injury remains poorly mapped. We studied 31 transplant recipients, integrating longitudinal T cell antigen receptor (TCR) profiling with single-cell RNA sequencing/TCR sequencing and spatial transcriptomics to track T cell clonal dynamics. We developed DecompTCR to resolve temporal dynamics and adapted computational tools to map clone phenotypes and niches in tissue. Our analyses revealed that cyclophosphamide selectively depletes alloreactive clones, although insufficient early expansion leads to incomplete depletion and severe disease. Severe graft‑versus‑host disease is marked by persistent expansion of alloreactive clones, rewiring of homeostatic cell types and diversification of donor-derived CD8 clonotypes that acquire Hobit (ZNF683) tissue‑resident memory T (T) cell programs during migration to epithelium. Spatial deconvolution identified CD8 effector/Hobit T hubs near intestinal stem‑cell-rich crypt bases and crypt‑loss regions. This clonotype‑resolved framework links tissue‑instructed T cell remodeling to localized epithelial injury, nominating early-repertoire dynamics and spatial hub burden as biomarkers.
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10. {"_":"ANKRD11 deficiency reprograms CD8 T cell differentiation to enhance immunity in chronic infection and cancer.","sup":["+"]}
PMID:日期:2026-09-11CD8 T cell dysfunction is a major obstacle to hepatitis B virus (HBV) clearance and antitumor immunity. Here, using a humanized mouse model, we identify a T cell receptor targeting a clinically relevant HBV epitope and reveal ANKRD11 as a key epigenetic regulator of CD8 T cell dysfunction in chronic infection and tumors. Ankrd11 knockout in CD8 T cells enhances HBV-specific T cell proliferation and effector differentiation, especially under immunosuppressive conditions, via AP-1 family gene upregulation. Loss of Ankrd11 both drives the conversion of progenitor exhausted T cells into terminally exhausted T cells, and reprograms PD-1TOX tolerant cells into functional effectors, improving antiviral and antitumor responses. Ankrd11-deficient T cells show increased granzyme and superior effector function, enhancing viral control and tumor regression. These findings position ANKRD11 as a promising immunotherapy target for chronic HBV infection and cancer.